SCOPE: Monocyte adhesion to the vascular endothelium is a crucial step in the early stages of atherogenesis. This study aims to investigate the capacity of an anthocyanin (ACN) and phenolic acid (PA) rich fraction (RF) of a wild blueberry, single ACNs (cyanidin, malvidin, delphinidin) and related metabolites (protocatechuic, syringic, and gallic acid) to counteract monocytes (THP-1) adhesion to human umbilical vein endothelial cells (HUVECs) in a tumor necrosis factor α (TNF-α) mediated proinflammatory environment. METHODS AND RESULTS: HUVECs were incubated with different concentrations (from 0.01 to 10 μg/mL) of the compounds for 24 h. Labeled monocytic THP-1 cells were added to HUVECs and their adhesion was induced by TNF-α (100 ng/mL). ACN-RF reduced THP-1 adhesion to HUVECs with a maximum effect at 10 μg/mL (-33%). PA-RF counteracted THP-1 adhesion at 0.01, 0.1, and 1 μg/mL (-45, -48.7, and -27.6%, respectively), but not at maximum concentration. Supplementation with gallic acid reduced THP-1 adhesion to HUVECs with a maximum effect at 1 μg/mL (-29.9%), while malvidin-3-glucoside and syringic acid increased the adhesion. No effect was observed for the other compounds. CONCLUSION: These results suggest that ACNs/PA-RF may prevent atherogenesis while the effects of the single ACNs and metabolites are controversial and merit further exploration.
SCOPE: Monocyte adhesion to the vascular endothelium is a crucial step in the early stages of atherogenesis. This study aims to investigate the capacity of an anthocyanin (ACN) and phenolic acid (PA) rich fraction (RF) of a wild blueberry, single ACNs (cyanidin, malvidin, delphinidin) and related metabolites (protocatechuic, syringic, and gallic acid) to counteract monocytes (THP-1) adhesion to human umbilical vein endothelial cells (HUVECs) in a tumor necrosis factor α (TNF-α) mediated proinflammatory environment. METHODS AND RESULTS: HUVECs were incubated with different concentrations (from 0.01 to 10 μg/mL) of the compounds for 24 h. Labeled monocytic THP-1 cells were added to HUVECs and their adhesion was induced by TNF-α (100 ng/mL). ACN-RF reduced THP-1 adhesion to HUVECs with a maximum effect at 10 μg/mL (-33%). PA-RF counteracted THP-1 adhesion at 0.01, 0.1, and 1 μg/mL (-45, -48.7, and -27.6%, respectively), but not at maximum concentration. Supplementation with gallic acid reduced THP-1 adhesion to HUVECs with a maximum effect at 1 μg/mL (-29.9%), while malvidin-3-glucoside and syringic acid increased the adhesion. No effect was observed for the other compounds. CONCLUSION: These results suggest that ACNs/PA-RF may prevent atherogenesis while the effects of the single ACNs and metabolites are controversial and merit further exploration.
Authors: Ioana Mozos; Corina Flangea; Daliborca C Vlad; Cristina Gug; Costin Mozos; Dana Stoian; Constantin T Luca; Jarosław O Horbańczuk; Olaf K Horbańczuk; Atanas G Atanasov Journal: Biomolecules Date: 2021-05-30